TY - JOUR. T1 - Monoclonal antibody to a nucleolar antigen of human B-lymphoblastoid cells. AU - Todorov, I. T.. AU - Philipova, R. N.. AU - Zhelev, N. Z.. AU - Hadjiolov, A. A.. PY - 1987/3. Y1 - 1987/3. N2 - An anti-nucleolar monoclonal antibody reacting with human B-lymphoblastoid cells but not with normal periferal blood lymphocytes has been isolated. The antibody recognized in Namalwa cells an antigen with molecular mass 41 kDa and pI 5.6, different from all previously described nucleolar antigens. Inhibition of rRNA transcription with Actinomycin D caused redistribution of the 41 5.6 antigen, but even at long term drug action it remains associated with the nucleolar remnants.. AB - An anti-nucleolar monoclonal antibody reacting with human B-lymphoblastoid cells but not with normal periferal blood lymphocytes has been isolated. The antibody recognized in Namalwa cells an antigen with molecular mass 41 kDa and pI 5.6, different from all previously described nucleolar antigens. Inhibition of ...
TY - JOUR. T1 - Direct effects of HP Acthar Gel® on human B lymphocyte activation in vitro. AU - Olsen, Nancy. AU - Decker, Dima A.. AU - Higgins, Paul. AU - Becker, Patrice M.. AU - McAloose, Carl A.. AU - Benko, Ann L.. AU - Kovacs, William. PY - 2015/10/27. Y1 - 2015/10/27. N2 - Introduction: Both clinical experience and experimental evidence have suggested that Adrenocorticotropic hormone (ACTH) might directly exert immunomodulatory effects not dependent on adrenal steroidogenesis. Methods: The direct effects of H.P. Acthar Gel® (Acthar), a repository preparation containing a porcine ACTH analogue, on human B lymphocyte function were studied in vitro using peripheral blood B cells isolated using anti-CD19 coated magnetic beads and activated by interleukin 4 (IL-4) and CD40 ligand (CD40L). Analysis of expression of messenger RNA (mRNA) encoding activation-induced cytidine deaminase (AICDA) was carried out by quantitative real-time polymerase chain reaction (PCR). Cellular proliferation was ...
TY - JOUR. T1 - CXCR5-dependent entry of CD8 T cells into rhesus macaque B-cell follicles achieved through T-cell engineering. AU - Ayala, Victor I.. AU - Deleage, Claire. AU - Trivett, Matthew T.. AU - Jain, Sumiti. AU - Coren, Lori V.. AU - Breed, Matthew W.. AU - Kramer, Joshua A.. AU - Thomas, James A.. AU - Estes, Jacob. AU - Lifson, Jeffrey D.. AU - Ott, David E.. PY - 2017/6/1. Y1 - 2017/6/1. N2 - Follicular helper CD4 T cells, TFH, residing in B-cell follicles within secondary lymphoid tissues, are readily infected by AIDS viruses and are a major source of persistent virus despite relative control of viral replication. This persistence is due at least in part to a relative exclusion of effective antiviral CD8 T cells from B-cell follicles. To determine whether CD8 T cells could be engineered to enter B-cell follicles, we genetically modified unselected CD8 T cells to express CXC chemokine receptor 5 (CXCR5), the chemokine receptor implicated in cellular entry into B-cell follicles. ...
Brezinschek, H.P., Brezinschek, R.I. & Lipsky, P.E., 1995, "Analysis of the Heavy Chain Repertoire of Human Peripheral B Cells Using Single-Cell Polymerase Chain Reaction", Journal of Immunology, 155:191-202 ...
Background. High serum levels and enhanced in vitro production of IgA are observed in more than half of patients with IgA nephropathy (IgAN); and transforming forming growth factor‐β (TGF‐β) is certain IgA class switching factor. On the other hand, macroscopic haematuria appears frequently with upper respiratory infection as tonsillitis in IgAN.. Methods. We compared the lymphocytic response to in‐vitro stimulation by group A streptococcal M proteins of apparent virulence factor between IgAN, non‐proliferative glomerulonephritis (NPGN), and normal subjects. M proteins were extracted from group A streptococcal strain type 5 and type 12 determined serologically.. Results. M protein‐induced proliferation of lymphocytes from IgAN was higher than in NPGN but not in healthy control subjects. Flow cytometric analysis indicated that stimulation by M protein extracts derived from type 5 streptococci (M5) increased surface IgA‐positive B cells in IgAN, but did not activate the production of ...
TY - JOUR. T1 - The role of B cell proliferation in the generation of immunoglobulin-secreting cells in man. AU - Jelinek, Diane F. AU - Lipsky, P. E.. PY - 1983. Y1 - 1983. N2 - The relationship of B cell proliferation and the generation of immunoglobulin-secreting cells (ISC) was explored in vitro by examining the effect of hydroxyurea (HU), an inhibitor of cellular DNA synthesis, on the generation of ISC from human peripheral blood mononuclear cells (PBM). HU completely inhibited the capacity of PBM to generate ISC in response to pokeweed mitogen (PWM) and other polyclonal B cell activators. Inhibition resulted from an effect on B cell proliferation, because HU also prevented the generation of ISC in cultures of purified B cells supplemented with either T cell supernatants or mitomycin C-treated T cells. Inhibiting B cell proliferation by treating them with mitomycin C before culture also abolished the generation of ISC. When ISC were enumerated after a 7-day incubation with PWM, the addition ...
Results Twenty patients were included. Nine were treated by etanercept (ETN), 9 by certolizumab pegol and 2 by adalimumab. The percentage of B cells significantly increased under TNFi from (median [IQR 25-75]) 4.6 (3.5-6.7) to 7.6 (5.2-9.9) % of lymphocytes. No change was observed in the different subtypes of B cells. However, in patients treated with ETN, IgD-CD27- double negative memory B cells significantly increased from 4.6 (2.5-5.4) to 7.7 (6.2-11.0)(p=0.03). The variation of those double negative B cells were significantly different from those observed with monoclonal antibodies (+1.6 [0.0-5.4] vs 0.3 [-1.3-1.8]% of B cells, p=0.02). No change of T, NK, NKT cells was observed in either group. EULAR responders at 3 months had significantly higher percentage of CD27+ memory B cells at baseline (32.9 [25.2-40.6] vs 19.5 [12.3-19.6]% of B cells, respectively; p=0.02), especially IgD+CD27+ pre-switch memory B cells (19.3 [9.8-21.8] vs 5.9 [4.9-9.4]% of B cells, respectively; p=0.02). Since ...
Interleukin 10 (IL-10) is a pleiotropic factor that enhances proliferation of activated human B lymphocytes and induces them to secrete high amounts of immunoglobulins. Here we show that several human B cell lines were able to constitutively secrete human (h)IL-10. Whereas none of the pre-B nor the plasmocytic cell lines tested produced hIL-10, 25 of the 36 tested mature B cell lines (lymphoblastoid and Burkitt lymphoma cell lines) secreted hIL-10. Moreover, 24 of these 25 hIL-10-producing B cell lines contained the Epstein-Barr virus (EBV) genome, suggesting a relationship between hIL-10 production by human B cell lines and EBV expression. Accordingly, whereas polyclonal activation via triggering of surface immunoglobulins or CD40 antigen induced highly purified normal human B lymphocytes to produce only low (0.3-0.4 ng/ml) but significant amounts of hIL-10, EBV infection induced them to secrete high amounts of hIL-10 (4-9 ng/ml). Furthermore, addition of exogenous hIL-10, simultaneously to EBV ...
We have been trying to get some MAIDS B cell tumors to grow in B6 mice. The tumors originally came from B6 mice but have been grown in tissue culture for several years. In the event we can not readapt them to grow in vivo we are in need of other tumors. If anyone has a B cell tumor, preferably before the plasma cell stage, and after the immature B cell stage that they have grown in B6 mice we would appreciate hearing about it. If it also grows in tissue culture, while being readly passed back into mice that would be a bonus. Please repond to this service or my email address:wiliam.wade at dartmouth.edu Thanks for your attention and help in this matter. Sincerely, William F. Wade, Ph.D. Assistant Professor of Microbiology Dartmouth Medical School ...
Schlegel, R A.; Von boehmer, H; and Shortman, K, "Antigen-initiated b lymphocyte differentiation. V. Electrophoretic separation of different subpopulations of afc progenitors for unprimed igm and memory igg responses to the nip determinant." (1975). Subject Strain Bibliography 1975. 1320 ...
CURRENT PROJECTS: - Using mouse genetics to identify the susceptibility factors that control B cell tolerance, differentiation and survival, leading to autoantibody production. - Defining the mechanisms by which autoimmune susceptibility elicits inflammation and recruitment of innate immune cells in secondary lymphoid organs that affect B cell function. - Examining helper activity and inflammatory cytokines of human T cells in peripheral blood of SLE patients that affect B cell function. - Characterizing the regulation and activity in primary mouse T follicular helper cells and T follicular regulatory cells to control B cell responses. - Defining the signal transduction events through the BCMA cytokine receptor that regulates both T follicular helper cell homeostasis and plasma cell survival in autoimmunity. - Characterizing the development and persistence of IgE antibodies to airway allergens. Go to Loren Ericksons Lab Site for detailed information about his lab and his research ...
Nonhomologous end-joining (NHEJ) repairs DNA double-strand breaks (DSBs) during V(D)J recombination in developing lymphocytes and during immunoglobulin (Ig) heavy chain (IgH) class switch recombination (CSR) in peripheral B lymphocytes. We now show that CD21-cre-mediated deletion of the Xrcc4 NHEJ gene in p53-deficient peripheral B cells leads to recurrent surface Ig-negative B lymphomas ("CXP lymphomas"). Remarkably, CXP lymphomas arise from peripheral B cells that had attempted both receptor editing (secondary V[D]J recombination of Igκ and Igλ light chain genes) and IgH CSR subsequent to Xrcc4 deletion. Correspondingly, CXP tumors frequently harbored a CSR-based reciprocal chromosomal translocation that fused IgH to c-myc, as well as large chromosomal deletions or translocations involving Igκ or Igλ, with the latter fusing Igλ to oncogenes or to IgH. Our findings reveal peripheral B cells that have undergone both editing and CSR and show them to be common progenitors of CXP tumors. Our ...
TY - JOUR. T1 - The CD40 ligand expressed by human B cells costimulates B cell responses. AU - Grammer, A. C.. AU - Bergman, M. C.. AU - Miura, Y.. AU - Fujita, K.. AU - Davis, L. S.. AU - Lipsky, P. E.. PY - 1995/1/1. Y1 - 1995/1/1. N2 - The possibility that activated B cells might express a ligand for CD40 that was of functional importance for B cell responses was examined by using highly purified human peripheral blood B cells, as well as a variety of B lymphoblastoid cell lines and hybridomas. Following stimulation with the combination of a calcium ionophore and a phorbol ester, human B cells bound a soluble fusion protein containing the extracellular portion of CD40 and the Fc region of lgG1 (CD40.lg). A variety of B cell lines and hybridomas also bound CD40.1g, either constitutively or after activation. In addition, CD40.Ig specifically immunoprecipitated a 33-kDa glycoprotein from surface 125I-labeled activated B cells. The nucleotide sequence of the coding region of the CD40 ligand mRNA ...
TY - JOUR. T1 - Splenic B cells and antigen-specific B cells process anti-Ig in a similar manner. AU - Myers, Christopher D.. AU - Vitetta, Ellen S.. PY - 1989. Y1 - 1989. N2 - B lymphocytes can process and present antigen to T cells. However, the fate of native antigen after its binding to specific B cells, i.e., the intracellular events involved in the processing and recycling of the antigenic fragments to the cell surface for antigen presentation, are not well understood. In the present study, we demonstrate that murine B cells degrade anti-Ig molecules bound to their surface and release acid soluble fragments into the supernatant. We also demonstrate that the kinetics of this process are identical for anti-μ, anti-δ, and anti-light chain antibodies, indicating that both surface IgM and surface IgD are equally effective in binding antigen and directing its processing. We also describe the effects of azide, chloroquine, and irradiation on this process. To extend these studies to the ...
Autoreactive B cells are activated in PGIA, but our understanding of how they contribute to disease susceptibility is incomplete. The present work provides direct evidence that B cells are essential for the development of arthritis and provides several different functions by which they contribute to disease. One of the major findings of our studies is that Ag presentation by B cells is critical for the activation of autoreactive T cells. Moreover, the APC function of B cells requires the direct recognition of Ag through the BCR to activate autoreactive T cells. Once activated, the autoreactive T cells can induce a very mild form of arthritis, indicating that T cells subsequent to activation by Ag-specific B cells have a direct pathogenic role in disease. Although DCs and macrophages are present in mIgM mice, they are not sufficient to function as APCs for autoreactive T cell activation. Our second major finding is that B cell production of autoantibody is critical and that autoantibodies alone ...
Mice with the autosomal recessive severe combined immune deficiency (scid) mutation lack mature lymphocytes because of defective joining of T cell receptor and immunoglobulin (Ig) gene segments. Penetrance of this mutation is incomplete since 10-25% of SCID mice produce some T or B lymphocytes. This "leaky" phenotype could be due to a reversion of the mutation in some mice or to a constant, low frequency of functional lymphocytes generated in all SCID mice with variable survival of such cells. We report here that all SCID mice can be stimulated to produce functional B cells by the transfer of normal neonatal, but not adult, T cells. T cell-induced rescue of C.B-17scid B cells results in high levels of Ig expressing the Ighb allotype of the SCID recipient. These results show that all SCID mice generate some functional B cells, the majority of which do not survive in the absence of a subset of T cells present in high frequency in the neonate ...
Intercellular adhesion molecule (ICAM) 1/CD54 plays an important role in T cell dependent B cell activation and for function of B lymphocytes as antigen-presenting cells. ICAM-1 expression is upregulated as a consequence of B lymphocyte antigen receptor (BCR) signaling, thereby serving to render antigen-stimulated B cells more receptive to T cell-mediated costimulatory signals. We have investigated BCR-induced expression of the Icam-1 gene in primary B cells and B cell lines and have found it to be dependent on BCR-induced expression of the transcription factor EGR1. Icam-1 transcription, induced by BCR cross-linking or bypassing the BCR with phorbol ester, is absent in a B cell line in which the EGR1-encoding gene (egr-1) is methylated and not expressed. A potential EGR1-binding site was located at -701 bp upstream of the murine Icam-1 gene transcription start site and shown by electrophoretic mobility shift assay to bind to murine EGR1. Mutation of this site in the context of 1.1 kb of the ...
Etiologic-based therapy is an ideal pharmacological option to treat or prevent diseases. There is no known etiology for multiple sclerosis (MS); however, envir...
Brown, L D.; Shen, F W.; Uhr, J W.; and Vitetta, E S., "The expression of lyb-2.1 On murine b lymphocytes. Abstr." (1978). Subject Strain Bibliography 1978. 1222 ...
Intraocular lymphoma is an aggressive non-Hodgkin B cell lymphoma involving the posterior eye. Basic research on this tumour has been hindered by an inability to expand the malignant B cell population. We developed a cell culture system, in which endothelial cell monolayers were infected with adenoviral vectors encoding HIV-1 proteins, Vpu and Tat. These monolayers permitted adhesion and proliferation of CD20-positive B cells from specimens of cerebrospinal fluid obtained from patients with intracranial tumor. The system provides a method for expansion of the malignant B cell population present in small volumes of fluid that are available for research use. ...
New insights into human B cell biology. B cells are highly important white blood cells known as lymphocytes and are part of the adaptive immune system. B cells have a specialised receptor on their cell surface (B cell receptor, BCR) which recognises specific proteins. Upon activation, B cells produce antibodies which bind antigens like e.g. molecules from pathogens or vaccines. The drawback of a vast range of different B cell receptors is the potential that some of the receptors recognise self-antigens which can then result in auto-immune disorders. The bone marrow continuously releases immature B cells into the blood stream. A high proportion of these so-called transitional B cells are able to recognise self-antigens via their BCR. It has been unknown where in the body these auto-reactive cells are checked and removed from the circulation. A recent publication by Anna Vossenkämper and Jo Spencer (Kings College) tracked the fate of human transitional B cells and identified that these cells ...
Infection with HIV drives significant alterations in B cell phenotype and function that can markedly influence antibody responses to immunisation. Anti-retroviral therapy (ART) can partially reverse many aspects of B cell dysregulation, however complete normalisation of vaccine responsiveness is not …
Sato S., Miller A.S., Howard M.C., Tedder T.F.. B lymphocyte development and function are regulated in part by the CD19 cell surface receptor complex, which is composed of at least four proteins; CD19, CD21 (CR2, complement receptor 2), CD81, and Leu 13. Because this complex has eight membrane-spanning domains and six cytoplasmic regions, determining the molecular basis for its function and signal transduction activities has not been straightforward. In this study, the contribution of the CD19 cytoplasmic domain to the in vivo function of the CD19/CD21/CD81/Leu 13 complex was assessed by generating CD19-deficient mice that expressed a transgene that encoded only the extracellular and transmembrane domains of CD19. Mice expressing this transgene were similar, if not identical, to CD19-deficient mice with abnormal B cell development, a lack of B-1 cells, increased surface IgM levels on B cells, modest mitogen responses, minimal serum Ig levels, and low humoral immune responses. The results of this ...
In this study we analyzed the effect of CD40 stimulation on the activity and nuclear appearance of Rel/nuclear factor kappaB (NF-kappaB) factors in primary murine B lymphocytes. We show that triggering of CD40 signaling pathway(s) by CD40 ligands expressed on L cells led to strong activation of an NF-kappaB-controlled beta-globin reporter gene in primary B lymphocytes from transgenic mice. Analyses of nuclear translocation of individual members of Rel proteins after CD40 induction of primary B cells showed a strong and long-lasting accumulation of RelB and, less pronounced, of c-Rel. LPS stimulation did not give rise to a persistent nuclear accumulation of RelB and c-Rel, whereas nuclear c-Rel, but not RelB, accumulated after B cell receptor stimulation. CD40 induced not only nuclear translocation but also de novo synthesis of RelB RNA and protein. S107 plasmacytoma cells, which express CD40 but are defective for the nuclear appearance of p50/p65-NF-kappaB, do not express RelB after CD40 stimulation. In
This report describes the effects of B cell growth factor (BCGFII) and other lymphokines in the differentiation of normal and tumor B cells. We compared BCL1 tumor B cells, normal B cells giving rise to a polyclonal response without the intentional addition of antigen, and an antigen-driven, SRBC-specific response. BCL1 tumor B cells gave maximum PFC responses when partially purified BCGFII was added or when suboptimal doses of BCGFII were mixed with one of several putative terminal differentiation factors we call B cell differentiation factors BCDF. IFN-gamma was not active as any of these factors. Maximum polyclonal responses of B cells were seen when either IL 2 or BCGFII were mixed with BCDF. In contrast, SRBC-specific responses showed a strict requirement for IL 2, and BCGFII and BCDF synergized with IL 2 to give a maximum response. The involvement of BCGFII in all of these responses suggests that BCGFII acts as a growth factor for a population of B cells that has differentiated much of the ...
We show here that approximately 25% of the mature peripheral B cells can survive in the mouse for at least 2 months without Syk, in a manner that requires BAFF‐R and CD19 signaling. In contrast, deletion of the Syk gene in early B cells results in the appearance of a small number of immature IgM+ B cells, which, however, fail to give rise to any mature B cells in the periphery (Cheng et al, 1995). Thus, pre‐B and mature B cells have different requirements for Syk. Indeed, the pre‐BCR is an autonomously signaling receptor that continuously engages Syk, whereas the BCR forms an autoinhibited oligomer on mature B cells that is not in contact with Syk. This notion is supported by a proximity ligation analysis showing that Syk is localized near the BCR only after BCR activation (Infantino et al, 2010; Klasener et al, 2014).. The presence of large amounts of Syk‐negative mature B cells in the induced mb1‐CreERT2;Sykfl/fl mice allowed us to analyze the in vivo role of this kinase in the ...
We show here that approximately 25% of the mature peripheral B cells can survive in the mouse for at least 2 months without Syk, in a manner that requires BAFF‐R and CD19 signaling. In contrast, deletion of the Syk gene in early B cells results in the appearance of a small number of immature IgM+ B cells, which, however, fail to give rise to any mature B cells in the periphery (Cheng et al, 1995). Thus, pre‐B and mature B cells have different requirements for Syk. Indeed, the pre‐BCR is an autonomously signaling receptor that continuously engages Syk, whereas the BCR forms an autoinhibited oligomer on mature B cells that is not in contact with Syk. This notion is supported by a proximity ligation analysis showing that Syk is localized near the BCR only after BCR activation (Infantino et al, 2010; Klasener et al, 2014).. The presence of large amounts of Syk‐negative mature B cells in the induced mb1‐CreERT2;Sykfl/fl mice allowed us to analyze the in vivo role of this kinase in the ...
We have used a novel hu-mouse model expressing a human-specific surrogate self-Ag to formally demonstrate that developing human B cells use receptor editing as a mechanism of central B cell tolerance. Central B cell tolerance in hu-mice is stringent but incomplete. Although the selection of autoreactive B cells into the periphery is rare, variations in the extent of tolerance were observed and shown to depend on the amount of self-Ag as well as the individual genetics of the source of CB.. To date, most studies of human B cell tolerance have focused on limited repertoire analyses of B cell subsets present in peripheral blood (Meffre and Wardemann, 2008; Meffre, 2011). These studies have been invaluable in establishing the presence of tolerance checkpoints, but they have been limited to a poorly defined set of self-Ags without a clear understanding of how these Ags directly affect B cells in vivo. In fact, although a significant reduction in the frequency of autoreactive clones in the human B ...
Redox-regulation of receptors and transcription factors are important for lymphocyte activation, differentiation and apoptosis. Thioredoxin (Trx) is a key redox-regulating protein and oxidative stress sensor operating in synergy with Trx-reductase and protein disulfide isomerase (PDI). The expression of Trx, PDI, and the Trx-regulated transcription-factor Pax5 were analyzed in a panel of human B cell lines and were compared with that of the Bcl-2 family proteins, also redox-controlled. The panel included representative cells from various stages: FLEB14-4 (pro-B), REH and NALM-6 (pre-B), Rael and Daudi (small mature B), U-698 and NC0467.3 (B-blasts), LP-1, U-1996, and U-266 (plasma cells). We found a significant congruence and co-variation of Trx and Bcl-2 levels in the B-lineage, with high expression levels in early stages (pro-B and pre-B) and in the late stage representing terminally-differentiated plasma cells, whereas mid-stage small resting B cells showed a very low expression. PDI ...
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The expression of the CD24 molecule, a glycoprotein expressed at the surface of most B lymphocytes and differentiating neuroblasts, was studied in developing nerve and muscle (after 16 weeks of gestat
A first clue that SPMs might affect B cell functions was the discovery that B cells express the ALX/FPR2 receptor that recognizes the D-series resolvins, RvD1 and RvD3 (79). 17-HDHA, RvD1, and PD1 are naturally produced within the spleen, a site where B cells commonly reside (35). PUFAs present in omega-3 fatty acid-rich fish oil (precursors for SPM production) were shown to affect B cell functions in mice by increasing antibody production and B cell activation (71, 72, 74). Similarly, mice fed a diet rich in DHA and EPA had a higher number of IgM-expressing splenic B cells following antigen stimulation compared with mice not receiving a PUFA-enriched diet (71). In a mouse model of diet-induced obesity, mice fed a high-fat (Western) diet containing primarily omega-6 fatty acids exhibited diminished antibody titers and increased mortality to influenza challenge relative to a normal diet. These effects could be rescued with dietary DHA (69). Dietary supplementation with PUFAs or PUFA-enriched fish ...
The production of antibody to a thymus-dependent Ag requires cooperation between the B cell and an Ag-specific Th cell. MHC restriction of this interaction implies that the Th cell recognizes Ag on the B cell surface in the context of MHC molecules and that the Ag-specific B cell gets help by acting as an APC for the Th cell. However, a number of studies have suggested that normal resting B cells are ineffective as APC, implying that the B cell must leave the resting state before it can interact specifically with a Th cell. Other studies, including our own with rabbit globulin-specific mouse T cell lines and hybridomas, show that certain T cell lines can be efficiently stimulated by normal resting B cells. One possible explanation for the above contradiction is that our B cells have become activated before presentation. Here we show that presentation by size-selected small B cells is not the result of nonspecific activation signals generated by the T cells or components of the medium. Also, although LPS
Normal B cells responsive to thymus independent-type 1 Ags (TI-1) are resistant to low doses of ionizing radiation in vivo (200-300 cGy), compared with TI-1 responsive B cells of mice with the CBA/N X-linked immunodeficiency (xid). This difference in radiosensitivity is an intrinsic B cell property; normal B cells adoptively transferred into xid mice remain TI-1-responsive after irradiation in situ. Because irradiation induces programmed cell death (PCD) in lymphocytes, we determined whether PCD were regulated differently in normal and xid B cells. B cells isolated immediately after irradiation from normal or xid donors when cultured without stimulators became apoptotic with the same kinetics and to the same extent, showing that apoptosis was induced equally in both populations. Apoptosis could be suppressed and mitogenesis could be induced frequently, however, if irradiated B cells were cultured with B cell activators. When activators using separate signal transduction pathways were compared, a
B lymphocytes are necessary cells in defense replies. B lymphocytes HVCN1S appearance is normally higher in B-cell lines and in B cells from sufferers with chronic lymphocytic leukemia where it could donate to disease pathogenesis. and and relationship did not differ significantly. HVCN1S Responds More Strongly Avasimibe Avasimibe to PKC-Dependent Phosphorylation. Proton currents in phagocytes and other cells are greatly augmented by phosphorylation of the channel by PKC (8). The enhanced gating response is usually stimulated effectively by the PKC activator PMA (phorbol myristate acetate) and is best analyzed using the perforated-patch configuration that preserves intracellular signaling pathways (9). Fig. 2 illustrates families of proton currents in cells expressing HVCN1L and HVCN1S before and after PMA activation. In response to PMA the currents turn on more rapidly and at more unfavorable voltages and turn off more slowly and the current amplitude is usually increased. Although HVCN1L ...
Ramos-Blue™ KD-MyD (MyD88 knockdown) is a B lymphocyte cell line specifically designed to monitor MyD88-mediated signaling.Ramos-Blue™ KD-MyD were obtained by stable integration of an NF-κB/AP-1-inducible SEAP (secreted embryonic alkaline phosphate) reporter gene and stable knowndown of the MyD88 ge
The HB14 monoclonal antibody reacts with human CD40, a 45-50 kDa type I transmembrane glycoprotein and member of the tumor necrosis factor receptor (TNFR) superfamily. It is expressed primarily on B cells, macrophages, follicular dendritic cells, endothelial cells, and fibroblasts and at lower levels on plasma cells and a subset of peripheral T cells. CD40 is involved in B cell differentiation and proliferation, isotype class-switching, and protection of B cells from apoptosis. Interaction of CD40 with its ligand CD154 is important in T cell-B cell interaction and plays a role in costimulation and immune regulation. Clone HB14 blocks the binding of CD40 to CD154. This prevents down-regulation of CD154 expression induced by interaction with CD40 expressed on antigen-presenting cells. - Belgique
Xu, H., Liew, L.N., Kuo, I.C., Huang, C.H., Goh, D.L.-M., Chua, K.Y. (2008). The modulatory effects of lipopolysaccharide-stimulated B cells on differential T-cell polarization. Immunology 125 (2) : 218-228. [email protected] Repository. https://doi.org/10.1111/j.1365-2567.2008.02832. ...
The CD38 antigen is a 45 kDa single chain type II integral membrane glycoprotein, with the NH2-terminus inside the cytoplasm. CD38 is an enzyme with several activities such as NAD glycohydrolase, ADP ribosylcyclase and cyclic ADP ribose hydrolase. CD38 is expressed on activated T and B lymphocytes, NK cells, monocytes, plasma cells and medullary thymocytes. CD38 expression appears to depend on the differentiation and activation of the cell. In the B cell lineage, CD38 is expressed in early stages of B-cell ontogeny, lost during maturation and re-expressed upon terminal differentiation to plasma cells. Similarly, CD38 is expressed on thymocytes and at a high level on activated T cells. Most mature resting lymphocytes of both B and T lineages do not express the CD38 antigen. CD38 is widely used as a marker to study T and B lymphocyte activation.
The CD38 antigen is a 45 kDa single chain type II integral membrane glycoprotein, with the NH2-terminus inside the cytoplasm. CD38 is an enzyme with several activities such as NAD glycohydrolase, ADP ribosylcyclase and cyclic ADP ribose hydrolase. CD38 is expressed on activated T and B lymphocytes, NK cells, monocytes, plasma cells and medullary thymocytes. CD38 expression appears to depend on the differentiation and activation of the cell. In the B cell lineage, CD38 is expressed in early stages of B-cell ontogeny, lost during maturation and re-expressed upon terminal differentiation to plasma cells. Similarly, CD38 is expressed on thymocytes and at a high level on activated T cells. Most mature resting lymphocytes of both B and T lineages do not express the CD38 antigen. CD38 is widely used as a marker to study T and B lymphocyte activation.
The CD38 antigen is a 45 kDa single chain type II integral membrane glycoprotein, with the NH2-terminus inside the cytoplasm. CD38 is an enzyme with several activities such as NAD glycohydrolase, ADP ribosylcyclase and cyclic ADP ribose hydrolase. CD38 is expressed on activated T and B lymphocytes, NK cells, monocytes, plasma cells and medullary thymocytes. CD38 expression appears to depend on the differentiation and activation of the cell. In the B cell lineage, CD38 is expressed in early stages of B-cell ontogeny, lost during maturation and re-expressed upon terminal differentiation to plasma cells. Similarly, CD38 is expressed on thymocytes and at a high level on activated T cells. Most mature resting lymphocytes of both B and T lineages do not express the CD38 antigen. CD38 is widely used as a marker to study T and B lymphocyte activation. *Alexa Fluor and Pacific Blue are registered trademarks of Molecular Probes, Inc ...
The CD38 antigen is a 45 kDa single chain type II integral membrane glycoprotein, with the NH2-terminus inside the cytoplasm. CD38 is an enzyme with several activities such as NAD glycohydrolase, ADP ribosylcyclase and cyclic ADP ribose hydrolase. CD38 is expressed on activated T and B lymphocytes, NK cells, monocytes, plasma cells and medullary thymocytes. CD38 expression appears to depend on the differentiation and activation of the cell. In the B cell lineage, CD38 is expressed in early stages of B-cell ontogeny, lost during maturation and re-expressed upon terminal differentiation to plasma cells. Similarly, CD38 is expressed on thymocytes and at a high level on activated T cells. Most mature resting lymphocytes of both B and T lineages do not express the CD38 antigen. CD38 is widely used as a marker to study T and B lymphocyte activation ...
Ofatumumab (oh" fa toom ue mab) is a human monoclonal IgG1 antibody to the cell surface antigen CD20 (also known as human B lymphocyte restricted differentiation antigen: Bp35), which is found on mature B cells as well as 90% of neoplastic B cell such as occur in chronic lymphocytic leukemia. CD20 is not present on pro-B cells, hematopoietic stem cells, normal plasma cells or other normal lymphocytes, circulating cells or tissues. Engagement of ofatumumab with CD20 leads to B cell lysis and depletion of circulating and tissue B cells for an extended period, up to 6 to 8 months. There is an accompanying mild decrease in IgM, but no change in IgG or IgA levels. ...
An assay for simultaneously determining the ratio of B cells and T cells to the total cell population and subpopulations thereof present in a lymphocyte population utilizes excess amounts of B cell bi
Enzymopathies are a disturbance of enzyme function, including genetic deficiency or defect in specific enzymes. Current methods for the treatment of enzymopathi...
Original citation: J. Clin. Invest.112:286-297 (2003). doi:10.1172/JCI18025.. Citation for this corrigendum: J. Clin. Invest.113:1069 (2004). doi:10.1172/JCI18025E1.. The legends for Figures 6 and 7 contained inaccuracies, and the correct versions appear below. The conclusions of the article are unaffected.. Figure 6 BAFF increases the generation of ISC from activated memory B cells. (a and b) Memory B cells were preactivated with CD40L and IL-2/IL-10 for 4 days and then recultured with (a) media (black bars), or (b) IL-2/IL-10 alone (black bars) or in the presence of CD40L (white bars) or BAFF (gray bars). Each value represents the mean Ig secretion ± SEM of five (a) or seven (b) experiments using cells from different donors. *P , 0.05; **P , 0.01. (c) Secondary B cell cultures were performed in the absence (black bars) or presence (white bars) of soluble TACI-Ig (20 μg/ml). The values represent the mean IgA ± SD of duplicate samples. (d) Memory B cells were preactivated with ...
Hi Jakub, I didnt get the original post, but I wanted to let you know about another method of Bcell stimulation that Ive used before- polyclonal goat anti-IgD. It was originally developed by Fred Finkelman (i think) and Ive used it in murine models in vivo systems with lots of luck- it should work in vitro if you can find the antibody. Interestingly, this type of stimulation is T cell independent, although it prefferentially activates naive B cells. IdGrad mbdxm at my-deja.com wrote: , Hi Jakub, , , Purify your B cells first then use PMA (phorbol , ester) 10 ug/ml and ionomycin 1 ug/ml. , , LPS should have worked but its not specific to B , cells. , , As for monkey anti-IgM ( anti-mu should be better), , try the antibody resource pages on the web there , are many usually as part of a company site. , , You might need to crosslink the anti-mu to get a , mitogenic signal. Even better if you stimulate your , cells with IL-4 and anti-IgM. , , cheers , , david , , In article ,382A22EC.D1A9E24F at ...
Antibody-producing B cells arise from hematopoietic stem cells through a series of developmental steps that involve a hierarchical transcription factor network....
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This gene was identified by the up-regulation of its expression upon Epstein-Barr virus infection of primary B lymphocytes. This gene is predicted to encode a G protein-coupled receptor that is most closely related to the thrombin receptor. Expression of this gene was detected in B-lymphocyte cell lines and lymphoid tissues but not in T-lymphocyte cell lines or peripheral blood T lymphocytes. The function of this gene is unknown ...